Systolic murmurs

Systolic murmurs of unknown cause should be evaluated by echocardiography.

Systolic heart murmur

Systolic heart murmurs are heart murmurs heard during systole.

Systolic heart murmurs are classified by when the murmur begins and ends, between S1 and S2.

Many involve stenosis of the semilunar valves or regurgitation of the atrioventricular valves.

Mid-systolic ejection murmurs are due to blood flow through the semilunar valves.

Causes of midsystolic ejection murmurs include outflow obstruction, increased flow through normal semilunar valves, dilation of aortic root or pulmonary trunk, or structural changes in the semilunar valves without obstruction.

Late systolic murmurs starts after S1 and, if left sided, extends up to S2, usually in a crescendo manner.

Late systolic murmurs causes include mitral valve prolapse, tricuspid valve prolapse and papillary muscle dysfunction.

Holosystolic murmurs start at S1 and extends up to S2

Holosystolic murmurs and are usually due to regurgitation in cases such as mitral regurgitation, tricuspid regurgitation, or ventricular septal defect (VSD).

Mid-systolic ejection murmurs can be due to aortic valve stenosis or hypertrophic cardiomyopathy with a harsh and rough quality.

Valvular aortic stenosis can produce a harsh, or even a musical murmur over the right second intercostal space which radiates into the neck over the two carotid arteries.

The most common cause of aortic stenosis is calcified valves due to aging.

The second most common cause is congenital bicuspid aortic valves as the normal valve is tricuspid.

Bicuspid aortic stenosis has little or no radiation, and it can be confirmed if it also has an aortic ejection sound, a short early diastolic murmur, and normal carotid pulse.

The murmur in ortic stenosis decreases with standing and straining with Valsalva maneuver.

Supravalvular aortic stenosis is may radiate more to the right carotid artery.

Subvalvular aortic stenosis is usually due to hypertrophic cardiomyopathy and its murmur is loudest over the left sternal border or the apex.

Subvalvular aortic stenosis murmur in hypertrophic cardiomyopathy increases in intensity with a standing position as well as straining with Valsalva maneuver.

Pulmonic stenosis associated with mid-systolic ejection murmur.

Pulmonic outflow obstruction murmur is a harsh murmur usually on left second intercostal space radiating to left neck and accompanied by palpable thrill.

Pulmonic outflow obstruction murmur can be distinguished from ventricular septal defect by listening to the S2, which is normal in ventricular septal defect, but it is widely split in pulmonary stenosis.

Ventricular septal defect is almost always pansystolic where the murmur of pulmonary stenosis is diamond-shaped and ends clearly before S2.

With many innocent murmurs S1 and S2 split normally.

Dilation of aortic root or pulmonary artery produces an ejection sound, with a short ejection systolic murmur and a relatively wide split S2.

A mid-systolic ejection murmur can be heard due to increased semilunar blood flow that can occur in anemia, pregnancy, or hyperthyroidism.

A mid-systolic ejection murmur may be due to aortic valve sclerosis from degenerative thickening of the roots of the aortic cusps but produces no obstruction and no hemodynamic instability and thus should be differentiated from aortic stenosis.

A mid-systolic ejection murmur may be due to aortic valve sclerosis that is heard over right second intercostal space with a normal carotid pulse and normal S2.

Innocent midsystolic murmurs are not accompanied by other abnormal findings.

Still’s murmur in children is such a benign murmur.

Late systolic murmur with mitral valve prolapse is the most common cause of late systolic murmurs.

Mitral valve prolapse murmur can be heard best over the apex of the heart, usually preceded by clicks.

The most common cause of mitral valve prolapse is floppy valve (Barlow’s) syndrome, and if the prolapse becomes severe enough, mitral regurgitation may occur.

Maneuvers that decrease left ventricular volume including: standing, sitting, Valsalva maneuver, and amyl nitrate inhalation can produce earlier onset of clicks, longer murmur duration, and decreased murmur intensity.

Maneuvers that increase left ventricular volume ― such as squatting, elevation of legs, hand grip, and phenylephrine ― can delay the onset of clicks, shorten murmur duration, and increase murmur intensity.

Late systolic murmur of tricuspid valve prolapse is uncommon without concomitant mitral valve prolapse.

Tricuspid valve prolapse is best heard over left lower sternal border.

Late systolic murmur of papillary muscle dysfunction is usually due to acute myocardial infarction or ischemia, which causes mild mitral regurgitation.

Holosystolic (pansystolic) murmurs.

Tricuspid regurgitation- Intensifies upon inspiration. Can be best heard over the fourth left sternal border. The intensity can be accentuated following inspiration (Carvallo’s sign) due to increased regurgitant flow in right ventricular volume.

Tricuspid regurgitation is most often secondary to pulmonary hypertension.

Primary tricuspid regurgitation is less common and can be due to bacterial endocarditis following IV drug use, Ebstein’s anomaly, carcinoid disease, or prior right ventricular infarction.

Holosystolic, pansystolic of mitral regurgitation.

Murmurs not intensified upon inspiration.

In the presence of incompetent mitral valve, the pressure in the L ventricle becomes greater than that in the L atrium at the onset of isovolumic contraction, which corresponds to the closing of the mitral valve (S1).

The murmur in MR starts at the same time as S1, and it can sometimes drown the sound of S2.

The murmur in MR is high pitched and best heard at the apex with diaphragm of the stethoscope with patient in the lateral decubitus position.

Left ventricular function can be assessed by determining the apical impulse, as a normal or hyperdynamic apical impulse suggests good ejection fraction and primary MR.

A displaced and sustained apical impulse suggests decreased ejection fraction and chronic and severe MR.

Holosystolic pansystolic murmur.

Ventricular septal defect has no intensification upon inspiration.

Ventricular septal defect occurs in the ventricular wall, producing a shunt between the left and right ventricles.

Since the L ventricle has a higher pressure than the R ventricle, flow during systole occurs from the L to R ventricle, producing the holosystolic murmur.

Ventricular septal defect is heard over the left third and fourth intercostal spaces and along the sternal border.

Ventricular septal defect is associated with normal pulmonary artery pressure and thus S2 is normal.

A normal S2 is used to distinguish from pulmonary stenosis, which has a wide splitting S2.

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